Saturday, April 14, 2018 High Point University Congdon School of Health Sciences Sponsored by: synapse.cofc.edu Schedule Time Event Room 8:00 Registration Lobby Breakfast Poster-Set-up 8:30 Opening Welcome Auditorium 8:45 - 9:45 Travel Awardees Oral Presentations Auditorium 10:00 - 11:00 Concurrent Session I Molecular Neurobiology Room 4090 and Drugs of Addiction Back-Yard-Brains Room 3027 11:00 - Noon Poster Session I Lobby Noon - 1:00 Buffet Lunch 2nd Floor Ballroom 1:00 - 2:00 Concurrent Session II Cognition/Behavior & Room 4089 Injury/Repair Back-Yard-Brains Room 3027 2:15 - 3:15 Poster Session II Lobby 3:15 - 3:45 Flex Time Campus Tour Steering Committee Room 2047 Poster Judging Room 2062 3:45 - 4:45 Keynote Address Auditorium 5:00 - 5:15 Closing and Awards Auditorium 2 Congdon Hall of Health Sciences FOURTH FLOOR 1 4 1 ANATOMY LAB 3 2 DEPT. OF PHYSICAL THERAPY ADMINISTRATION 4089 3 MEDICINAL AND PHARMACEUTICAL CHEMISTRY 4090 RESEARCH LAB 2 5 4 PHARMACOLOGY RESEARCH LAB 5 FRED WILSON SCHOOL OF PHARMACY FACULTY OFFICES 3 THIRD FLOOR 4 7 1 DEPT. OF PHYSICIAN 6 STANDARDIZED 5 6 ASSISTANT STUDIES CLIENT SUITE 2 ADMINISTRATION 3027 7 INFECTIOUS 2 SIMULATION LABS DISEASE LAB 1 8 3 CLINICAL SKILLS LAB 8 FRED WILSON SCHOOL OF 4 HISTORY AND PHARMACY PHYSICAL EXAM LAB ADMINISTRATION 5 BALLROOM SECOND FLOOR 2 1 LOBBY 3 4 2047 2 PHYSICAL THERAPY NEUROSCIENCE LAB 3 VIRTUAL REALITY AND GAIT ANALYSIS LAB 2062 1 5 4 PHARMACY SKILLS LABORATORY SUITE 5 CALLICUTT AUDITORIUM FIRST FLOOR 1 HUMAN BIOMECHANICS AND PHYSIOLOGY LAB 1 2 2 WILLED BODY PROGRAM 3 3 PHARMACY COLLABORATION SPACES AND 4 CLASSROOMS 4 MUSCULOSKELETAL LAB HIGHPOINT.EDU 3 Notes 4 Keynote Speakers Dr. Read Montague holds professorships in Physics at Virginia Tech, and in Psychiatry and Behavioral Medicine at Virginia Tech School of Medicine. He is the Director of both the Human Neuroimaging Laboratory and the Compu- tational Psychiatry Unit at Virginia Tech Carilion Research Institute where his team uses computational and experimental approaches to study decision-making, addiction, social exchanges, and the role of specific neurotransmitters and brain regions in cognition within normal and diseased patients. Dr. Montague is well regarded for his national and international speaking engagements, and his work has been featured on PBS’s “The Brain with David Eagleman,” in a Global TED talk, and in numerous scientific and popular articles. Tim Marzullo, co-founder of Back-Yard-Brains, specializes in Neu- ro-Engineering with doctorate of Neuroscience from the University of Michigan. Before synthesizing and developing Back Yard Brains, Tim was a Lecturer at the University of Michigan and a research Engineer for NeurNexus Technologies, thus his “path to success” will be familiar, yet inspiring to students. His company is federally funded (National Institutes of Mental Health SBIR grant: -#2R44MH093334-03: Backyard Brains: Bringing Neurophysiology into secondary schools) and focused on outreach and neuroscience education. 5 Plenary Session — Travel Awardee Oral Presentations 1. Waugh, C. Escobedo, C. Kalantar, A. Ford, B. 2. Eppley KJ, Faust-Casey BK, Goodman JI, Gosine AE, Kraemer, B. Department of Biological Sciences, Bruce AA, Wilhelm JC. Department of Biology, Department Eastern Kentucky University of Psychology, Program of Neuroscience, College of Charles- ton, Charleston, SC Activation of the p75 Neurotrophin Receptor in Degenerating Dopaminergic Neurons Subjected to Effects of Estrogen on Sensory Neuron Participation in Axon Oxidative Stress Regeneration Following Peripheral Nerve Injury. The p75 neurotrophin receptor is a transmembrane protein Peripheral nerve injuries affect hundreds of thousands of people that promotes the death of neurons affected by various injuries each year in the United States alone. Despite the fact that periph- or pathological conditions. Tissue damage can lead to upreg- eral nerves have the ability to regenerate, functional recovery is ulation of pro-neurotrophins, ligands that bind and activate often very poor due to insufficient axon regeneration. Previous p75NTR. Upon activation, p75NTR is cleaved by TNF-α studies have shown that treatment with estrogen can significantly Converting Enzyme (TACE) and the gamma-secretase com- enhance the regeneration of motoneurons following peripheral plex, thereby releasing the intracellular domain of the recep- nerve injury; however, this has not yet been studied in sensory tor to activate downstream pro-apoptotic mediators. From neurons. Both sensory and motoneuron regeneration are nec- previous analyses of sympathetic neurons, we discovered that essary in order to obtain full functional recovery; therefore, the cleavage of p75NTR is induced by oxidative stress, a cellular present study examined the role of estradiol signaling in sensory condition associated with numerous types of pathological neuron participation and hypothesized that systemic estrogen conditions. Surprisingly, however, this mechanism of receptor treatment will increase the rate of axon regeneration in sensory activation did not require neurotrophins. Thus, ligand-inde- neurons following peripheral nerve injury. Male and female mice pendent activation of p75NTR in neurons subjected to oxida- were anesthetized and the common fibular branch of the right tive stress may underlie the ability of the receptor to promote sciatic nerve was cut and repaired using fibrin glue. Immediately degeneration of cells affected by a wide variety of pathological after transection surgery, mice were treated for two weeks with conditions. Whether oxidative stress-induced p75NTR activa- either estradiol-filled or unfilled (blank) capsules inserted in the tion contributes to neurodegeneration in the central nervous nape of their neck. Upon completion of estradiol or control system has not been explored. In the present study, we evaluate treatments, animals underwent a second surgery during which the contribution of p75NTR to oxidative stress-induced de- a retrograde tracer was applied 1.5mm distal to the original generation of midbrain dopaminergic neurons, a population of repair site in order to label the sensory neurons whose axons had cells particularly susceptible to Parkinson’s disease. To overcome regenerated at least that distance. Three days following retrograde limitations of primary cultured dopaminergic neurons for pro- labelling, all animals were sacrificed, and regeneration was quan- tein analysis, these investigations were conducted using LUH- tified by counting the number of neurons containing fluorescent MES cells, a population of conditionally-immortalized human tracer dye. Systemic estradiol treatment significantly increased the mesencephalic cells that can be differentiated to post-mitotic, number of labelled axons, and therefore indicates an increase in electrically active cells with morphological features and protein sensory neuron participation in axon regeneration. These findings expression profiles resembling mature dopaminergic neurons. demonstrate the ability of sensory axons to regenerate in a similar We have discovered that these dopaminergic cells abundantly manner as motoneurons, and show that estrogen treatment can express p75NTR and are susceptible to oxidative stress-asso- be used to increase the likelihood of full functional recovery ciated death induced by 6-hydroxdopamine (6-OHDA), a following peripheral nerve injury. compound commonly used to mimic the effects of Parkinson’s disease. Exposure of differentiated LUHMES cells to 6-OHDA resulted in proteolysis of p75NTR. Our preliminary analyses 3. Carter JS, Kearns AM, Weber RA, Reichel CM. also indicate that oxidative stress-induced cleavage of p75NTR Department of Biology, College of Charleston in dopaminergic cells does not require neurotrophins. Thus, ligand-independent stimulation of p75NTR proteolysis may Long term impact of acute stress on cognition, anxiety, and contribute to oxidative stress-associated degeneration of do- reinstated heroin seeking in male and female rats. paminergic neurons. Future studies will further elucidate the mechanisms through which p75NTR is activated by oxidative It has been suggested that withdrawal symptoms following stress, as well as evaluate the contributions of the receptor to substance use disorders (SUD) and post-traumatic stress disorder dopaminergic neurodegeneration. (PTSD) reciprocally exacerbate one another. Withdrawal symp- 6 toms, induced by cessation of substance abuse behavior, culmi- reward pathway, incentivizes certain behaviors and discourages nate as stressors and lead to persistent and compulsive relapse others by varying dopamine levels. Recently, a novel area known behavior. In addition, PTSD can be triggered by, and contrib- as the rostromedial tegmental nucleus (RMTg) was found to ute to, withdrawal-induced stress responses further increasing send a inhibitory GABAergic projection to the reward pathway. relapse potential. Previous work has shown that rats potentiate Therefore, the RMTg has been indicated as a potential “brake” substance-seeking behavior when exposed to scents associated mechanism for this well-researched circuit. Past research shows with restraint stress, a model used to mimic PTSD in rodents. that inactivation of the RMTg through Designer Receptors We examined the effects of restraint stress on heroin seeking and Exclusively Activated by Designer Drugs (DREADDs) increases anxiety related behaviors during withdrawal in male and female self-administration in rats in the presence of negative stimuli,